Published on 19/03/2015 by admin
Filed under Dermatology
Last modified 22/04/2025
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Dana Turker and Jacob O. Levitt
Evidence Levels: A Double-blind study B Clinical trial ≥ 20 subjects C Clinical trial < 20 subjects D Series ≥ 5 subjects E Anecdotal case reports
Papular urticaria (PU) is a common disease characterized by chronic or recurrent eruptions of 3–10 mm pruritic papules, wheals, and/or vesicles caused by hypersensitivity to the bites of arthropods, including fleas, mosquitoes, scabies, and bedbugs. Not all individuals who are bitten by an offending arthropod develop a reaction to the bite. However, when a bite reaction resulting in a papular skin eruption does occur, this is defined as papular urticaria. Although the antigenic stimulus cannot be identified in all cases, an eosinophilic infiltrate on histology supports that etiology. Papules tend to appear on extensor surfaces of the extremities and may have a central punctum; lesions last between 2 and 10 days. Excoriations, lichenification, and secondary infection are often noted. Cases are generally seen in children between the ages of 2 and 7 and in adults, with a predilection for the spring and summer months.
Bed bugs (Cimex lectularius) are an increasingly common cause of PU. They live in wallpaper, mattress seams, couches, and headboards but can also be found in luggage, vehicles, and clothing. Importantly, they can live off of the host up to 1 year after just one blood meal and can be spread via used furniture as well as travelers (clothing, baggage). They feed at night for 4 to 12 minutes and typically cause a painless bite of which the host is unaware. Bed bugs are detected via human inspection, bed bug sniffing dogs, and CO2-emitting monitoring systems. In conjunction with chemical treatment of the home, the following strategies can be used to prevent further infestation: a sealed, plastic cover for the mattress, moving the mattress away from the wall, keeping blankets off the floor, petrolatum applied to the legs of the bed, plastic cups under the legs of the beds, white sheets to make the bed bugs and/or blood more visible, removing loose wallpaper, and filling in cracks in floorboards, furniture, walls, and windowsills. Travelers should examine the bed, avoid using hotel drawers, keep suitcases zipped, and launder clothes with heated drying upon return.
The exact cause of PU is often not found and thus it is a diagnosis of exclusion. Common causes are bed bugs, scabies, lice (all types), fleas, chiggers, and mosquitoes. Important differential diagnoses to consider are prurigo nodularis, allergic contact dermatitis, id reaction, atopic dermatitis, drug rash, urticaria, sarcoidosis, early varicella, pityriasis lichenoides, miliaria rubra, papulovesicular polymorphous light eruption, papular acrodermatitis of childhood (Gianotti–Crosti syndrome), linear IgA bullous dermatosis, folliculitis, delusions of parasitosis, and neurotic excoriations.
We suggest a therapeutic ladder based on simultaneously addressing: (1) a presumed arthropod assault; (2) the pathophysiology of the allergic and inflammatory response; and (3) the severity of the inflammation at presentation.
Most important is the identification and removal of the offending arthropod, which may require intense investigation as to the possible sources. Because the risks are minimal and the benefit great, empiric therapy for scabies should be given. This can be achieved with permethrin cream 5% or malathion lotion 0.5% done once and repeated 3 to 7 days later. In the case of suspected bed bugs and fleas, fumigation of the home is required using professional services. Fumigation of the home should also be considered in recurrent cases of PU. Clothes and bedding should be laundered before and after treatment; specifically, placed in a dryer at 60°C for 10 minutes to dehydrate and kill scabies and bed bugs. In persistent cases, application of DEET before bed may help. If there are pets in the home, aggressive flea control and veterinary evaluation may be necessary. If the exposure is thought to be from the outdoors, prevention can be achieved through protective clothing and insect repellents.
While the cause of PU is being investigated and treated, symptomatic therapy should be implemented immediately for patient comfort and to reduce and prevent inflammation. For mild cases, topical steroids should be prescribed, with choice of class depending on the severity of lesions. For individual refractory or severe lesions, intralesional triamcinolone is often helpful. When steroids fail or if inflammation is severe on initial presentation, proceed to systemic immunosuppression; for example, a 10-day oral prednisone taper starting at 1 mg/kg or 1 mg/kg of intramuscular triamcinolone. When PU becomes chronic in the context of two failed courses of systemic steroids and negative pest control investigations, other diagnoses and/or systemic immunosuppressants should be considered, e.g., phototherapy, cyclosporine, or methotrexate.
Antihistamines often control pruritus. In milder cases, non-sedating antihistamines such as loratadine, desloratidine, fexofenadine, cetirizine, or levocetirizine can help. Doses above those given on the product labeling may be necessary. With more severe itching, diphenhydramine and hydroxyzine are favored. In chronic or recurrent cases, T-cell mediated lesions, in contrast to the histamine-mediated lesions of early PU, may render antihistamines ineffective. In that case, topical agents, such as camphor/menthol, calamine lotion, crotamiton, lidocaine, and pramoxine, can help. Secondary infection, often from scratching, is a concern, especially in children, and appropriate topical or oral antibiotics should be used.
Complete blood count with differential
Serum IgE
Skin biopsy (if systemic treatment is being given)
Environmental evaluation
Scratch test for dermographism
Jordaan HF, Schneider JW. Am J Dermatopathol 1997; 19: 119–26.
Over half the cases had mild acanthosis, mild spongiosis, exocytosis of lymphocytes, mild subepidermal edema, extravasation of erythrocytes, a superficial and deep mixed inflammatory cell infiltrate of moderate intensity with interstitial eosinophils. Four subtypes are described: lymphocytic, eosinophilic, neutrophilic, and mixed. The authors conclude that a type I hypersensitivity reaction is part of the pathogenesis of PU based on immunohistochemical evidence.
Peng Z, Beckett AN, Engler RJ, Hoffman DR, Ott NL, Simons FE. J Allergy Clin Immunol 2004; 114: 1189–94.
When compared to healthy controls, children with a known allergy to mosquito bites had higher mosquito-directed IgE antibody levels in their saliva.
Cuéllar A, Rodríguez A, Halpert E, Rojas F, Gómez A, Rojas A, et al. Allergol Immunopathol (Madr) 2010; 38: 197–202.
Those children (clinically diagnosed with PU due to flea bites) who had experienced 2 to 5 years of symptoms responded to flea antigen with higher IgE bands than did children with either a shorter or longer duration of symptoms. Healthy controls responded to the flea antigen mainly with IgG1 and IgG3.
Howard R, Frieden IJ. Pediatr Dermatol 1996; 13: 246–9.
Definitive treatment is the elimination of the arthropod source. Pets must be treated with insecticidal shampoos and be well-groomed. Carpets, rugs, and cloth furniture should be thoroughly vacuumed and the vacuum bag disposed of. Fumigation of fleas should include outdoor areas that the pet frequents.
Theis J, Lavoipierre MM, LaPerriere R, Kroese H. Arch Dermatol 1981; 117: 341–3.
Six cases of PU caused by the tropical rat mite (Ornithonyssus bacoti) are presented. Rodents were present in or around the home in most cases. Patients were treated successfully with lindane, and exterminators were used to completely rid the source.
Bolam RM, Burtt ET. Br Med J 1956; 1(4976): 1130–3.
Evidence of fleas was found in 21 of 30 cases of PU. Careful histories were taken, and home visits were done in most cases because the source was not apparent. Insecticides were advised to clear any pets of fleas, and the owners were encouraged to have a specified rug or area where the pet sleeps. This area should be cleaned regularly with insecticide dust.
Karppinen A, Kautiainen H, Petman L, Burri P, Reunala T. Allergy 2002; 57: 534–7.
A double-blind, placebo-controlled, crossover study comparing prophylactic daily cetirizine 10 mg, ebastine 10 mg, and loratadine 10 mg in 29 adults with mosquito bites. Cetirizine and ebastine significantly reduced the size of wheals and pruritus. Cetirizine was found to be most effective against pruritus but caused sedation more often than did ebastine and loratadine.
Karppinen A, Brummer-Korvenkontio H, Petman L, Kautiainen H, Herve JP, Reunala T. Acta Derm Venereol 2006; 86: 329–31.
A double-blind, placebo-controlled, crossover study with levocetirizine 5 mg daily in 28 adults sensitive to mosquito bites. Patients were given the study drug for 4 days and exposed to mosquito bites on day 3. Levocetirizine reduced the size of wheals by 60% and pruritus by 62% compared to placebo.
Dilaimy M. Cutis 1978; 21: 666–8.
The author reports a good response with oral antihistamines after 10 to 14 days in an Iraqi population of patients with bullous papular urticaria.
Pillsbury DM, Constant ER. Arch Dermatol Syphilol 1948; 57: 410–11.
Case report of a 6-year-old boy with PU who had improvement of symptoms within 20 minutes of administration of diphenhydramine. He had an 80% improvement after 1 week of treatment and showed the development of new lesions at a more rapid rate upon withdrawal of diphenhydramine.
Steen CJ, Carbonaro PA, Schwartz RA. J Am Acad Dermatol 2004; 50: 819–42.
The authors advocate identification and removal of the cause of PU while simultaneously treating symptoms with topical steroids and oral antihistamines.
A good review of arthropods and the cutaneous eruptions they can cause.
Naimer SA, Cohen AD, Mumcuoglu KY, Vardy DA. Isr Med Assoc J 2002; 4: 911–13.
Twenty patients with PU caused by cat fleas (Ctenocephalides felis) are presented. Symptomatic control was achieved with calamine lotion, topical corticosteroids, and oral antihistamines. Clinical symptoms cleared within a few weeks after fumigating and spraying the areas infested by arthropods.
Millikan LE. Semin Dermatol 1993; 12: 53–6.
Prevent PU using repellents containing DEET if repeated exposure is suspected. Use antipruritics, including menthol, camphor, and pramoxine for pruritus.
Wang C, Tsai WT, Cooper R, White J. J Econ Entomol 2011; 104: 274–8.
The authors compared the effectiveness of three bed bug monitoring devices containing CO2 as an attractant. They found that, on a daily basis, a home-made dry ice trap was most effective, followed by CDC3000 and then NightWatch; however, when NightWatch was used consecutively over many nights, its efficacy increased. The study also confirmed the use of the attractant-less monitor, Interceptor, as an effective device; its efficacy over 7 days was similar to the one-day efficacy of dry ice traps. Over the span of 1 day in lightly infested apartments, the detection rates for the dry ice trap, CDC3000, and NightWatch were 60%, 50%, and 10%, respectively. When the Interceptor was used over 7 days, it detected 70% of light infestations and 100% of heavy infestations.
Pfiester M, Koehler PG, Pereira RM. J Econ Entomol 2008; 101: 1389–96.
Dogs trained to detect bed bugs and viable bed bug eggs via olfaction correctly identified bed bugs placed into vented polyvinyl chloride containers with a 97.5% positive indication rate and 0% false positive rate. In a controlled experiment set-up in hotel rooms, the dogs were able to detect the bed bugs with 98% accuracy.
Pereira RM, Koehler PG, Pfiester M, Walker W. J Econ Entomol 2009; 102: 1182–8.
Heat treatment of furniture for 2 to 7 hours at 49°C using equipment that costs less than $400 can successfully disinfect furniture (negating the need to throw out the furniture).
Gibbs SG, Lowe JJ, Smith PW, Hewlett AL. Infect Control Hosp Epidemiol 2012; 33: 495–9.
At all concentrations tested (362, 724, and 1086 ppm) chlorine dioxide resulted in 100% mortality of bedbugs 18 hours after the exposure. These concentrations can be safely achieved in a hospital room.
Hernandez RG, Cohen BA. Pediatrics 2006; 118: 189–96.
Authors advocate the use of intralesional steroids in older children and adults to suppress pruritus if more conservative measures fail.
El-Nasr NS. J Egypt Med Assoc 1961; 44: 340–1.
Dexamethasone 0.25 mg PO two to three times daily for 1 to 2 weeks was used with good results. Pruritus resolved within 48 hours.
Kumar S, Prakash S, Rao KM. Indian J Med Res 1995; 102: 20–3.
Diethyl-m-toluamide (DEET), diethylphenyl acetamide and dimethylphthalate were tested against bedbugs Cimex hemipterus on the shaven skin of rabbits. DEET was superior to the other two repellents at all concentrations tested. At 75% concentration, DEET showed 85% repellency for up to 2 hours and 52% repellency 6 hours after treatment.
Brown M, Hebert AA. J Am Acad Dermatol 1997; 36: 243–9.
DEET was highly effective at repelling mosquitoes, biting fleas, gnats, chiggers, and ticks. Permethrin works as both an insecticide and a repellent against lice, ticks, fleas, mites, mosquitoes, and black flies.
Sherertz EF. J Am Acad Dermatol 1991; 24: 697–702.
Twelve patients with pruritic papular eruptions were followed, and the majority were refractory to conservative symptomatic management but showed some control with oral steroids, UVB or PUVA.
Smith SR, Macfarlane AW, Lewis-Jones MS. Clin Exp Dermatol 1988; 13: 260–2.
A 20-year-old male who underwent allogenic bone marrow transplant was found to have PU as a result of transfer of allergy from the donor. The PU eruption appeared as cyclosporine was withdrawn, indicating a suppressive effect on PU from cyclosporine.
Treatment of Skin Disease Comprehensive Therapeutic Strategies 4e
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Elimination of arthropod
Antihistamines
Topical steroids
Topical antipruritics, e.g., camphor/menthol, calamine lotion, crotamiton, lidocaine, and pramoxine
Intralesional steroids, e.g., triamcinolone
Oral steroids, e.g., prednisone or methylprednisolone
Insect repellents, i.e., DEET
Phototherapy
Cyclosporine
Hospitalization
